I. BACTERIAL PATHOGENESIS

B. VIRULENCE FACTORS THAT PROMOTE BACTERIAL COLONIZATION OF THE HOST

6. The abilty to evade adaptive immune defenses

The overall purpose of this Learning Object is:
1) to learn how the ability to resist adaptive immune defenses plays a role in bacterial pathogenicity by promoting colonization; and
2) to introduce several examples of medically important bacteria that are able to resist certain adaptive immune defenses in order to promote colonization.

LEARNING OBJECTIVES FOR THIS SECTION

In this section on Bacterial Pathogenesis we will be looking at virulence factors that promote bacterial colonization of the host. The following are virulence factors that promote bacterial colonization of the host .

1. The ability to use motility and other means to contact host cells.
2. The ability to adhere to host cells and resist physical removal.
3. The ability to invade host cells.
4. The ability to compete for iron and other nutrients.
5. The ability to resist innate immune defenses such as phagocytosis and complement.
6. The ability to evade adaptive immune defenses.

We will now look at the ability of bacteria to evade adaptive immune defenses.

6. The Ability to Evade Adaptive Immune Defenses

One of the major defenses against bacteria is the immune defenses' production of antibody molecules (def) against the organism. The "tips" of the antibody (the Fab portion; see Fig. 1) have shapes that have a complementary shape to portions of bacterial proteins and polysaccharides called epitopes (def. The "bottom" of the antibody (the Fc portion; see Fig. 1) binds to receptors on phagocytes and NK cells (def)) and can activate the classical complement pathway (def).

There are various ways antibodies made during adaptive immunity protect the body against bacteria:

a. As mentioned above under phagocytosis, some antibodies such as IgG and IgE function as opsonins (def) and stick bacteria to phagocytes (see Fig. 2).

Flash animation illustrating the function of enhanced attachment by way of IgG.

b. Antibodies, such as IgG, IgA, and IgM, can bind to bacterial adhesins, pili, and capsules and in this way block their attachment to host cells.

Flash animation showing antibodies blocking bacterial adherence to host cell.

c. IgG and IgM can also activate the classical complement pathway (def) providing all of its associated benefits.

d. IgA and IgM can clump bacteria together enabling them to be more readily removed by phagocytes (see Fig. 1).

These mechanisms will be discussed in greater detail in Unit 5.

For More Information: Antibodies from Unit 5

 

Bacteria utilize a variety of mechanisms to resist antibodies made during adaptive immunity. These include the following:

• Certain bacteria can evade antibodies is by changing the adhesive tips of their pili (def) as mentioned above with Neisseria gonorrhoeae (inf) as seen in Fig. 3. Bacteria can also vary other surface proteins so that antibodies already made will no longer "fit."
• N. gonorrhoeae produces Rmp protein (protein III) that protects against antibody attack by antibodies made against other surface proteins (such as adhesins) and the lipooligosaccharide (LOS) of the bacterium.
• Neisseria meningitidis (inf) has a capsule (def) composed of sialic acid while Streptococcus pyogenes (group A beta streptococci) (inf) has a capsule made of hyaluronic acid. Both of these polysaccharides closely resemble carbohydrates found in human tissue polysaccharides and because they are not recognized as foreign by the lymphocytes that carry out the immune responses, antibodies are not made against these capsules. Likewise, some bacteria are able to coat themselves with host proteins such as fibronectin, lactferrin, or transferrin and in this way avoid antibodies.
• Staphylococcus aureus (inf) produces protein A while Streptococcus pyogenes (inf) produces protein G. Both of these proteins bind to the Fc portion of antibodies (see Fig. 1) and in this way the bacteria become coated with antibodies in a way that does not result in opsonization (see Fig. 4).
• Salmonella species can undergo phase variation of their capsular (K) and flagellar (H) antigens, that is, they can change the molecular shape of their capsular and flagellar antigens so that antibodies made against the previous form no longer fit the new form.
• Bacteria such as Haemophilus influenzae (inf), Streptococcus pneumoniae (inf), Helicobacter pylori (inf), Shigella flexneri (inf), Neisseria meningitidis (inf), Neisseria gonorrhoeae (inf) and enteropathogenic E. coli (inf) produce immunoglobulin proteases. Immunoglobulin proteases degrade the body's protective antibodies (immunoglobulins) that are found in body secretions, a class of antibodies known as IgA.

• Many pathogenic bacteria, as well as normal flora, form complex bacterial communities as biofilms. Bacteria in biofilms are often able to communicate with one another by a process called quorum sensing (discussed later in this unit) and are able to interact with and adapt to their environment as a population of bacteria rather than as individual bacteria. By living as a community of bacteria as a biofilm, these bacteria are:

  1. better able to resist attack by antibiotics, and

  2. are better able to resist the host immune system.

  For further information on bacterial pathogenesis, see the online Microbiology Web Textbook at the University of Wisconsin-Madison.

   

E-Medicine article on infections associated with organisms mentioned in this Learning Object. Registration to access this website is free. Neisseria gonorrhoeae Neisseria meningitidis Streptococcus pyogenes Staphylococcus aureus Haemophilus influenzae Streptococcus pneumoniae Helicobacter pylori Shigella species Escherichia coli

• QUIZ YOURSELF ON THIS SECTION

Doc Kaiser's Microbiology Home Page
Copyright © Gary E. Kaiser
All Rights Reserved
Updated: Feb., 2009
Please send comments and inquiries to Dr. Gary Kaiser